Psychological stress weakens the ability of certain immune cells to clear away dead cells, causing a buildup that triggers more inflammation and worsens allergic reactions
Study: Stress-experienced monocytes/macrophages lose anti-inflammatory function via β2-adrenergic receptor in skin allergic inflammation. Image Credit: savitskaya iryna / Shutterstock.com
A recent Journal of Allergy and Clinical Immunology study investigates the cellular and molecular mechanisms through which stress exacerbates immunoglobulin E cutaneous allergic inflammation (IgE-CAI).
How does psychological stress impact disease risk?
Stress activates the hypothalamic-pituitary-adrenal axis and sympathetic nervous system (SNS), which subsequently induces the systemic release of epinephrine, norepinephrine, and glucocorticoids (GCs) from the adrenal gland and sympathetic postganglionic neurons.
Most immune cells express the receptors for epinephrine, norepinephrine, and GCs, all of which are stress hormones that can increase heart rate and blood pressure levels. Previous studies have also demonstrated that alterations in these hormone levels can influence immune responses.
GCs and catecholamines inhibit the TH1 response, which causes apoptosis and, as a result, altered immune cell dynamics. This stress response has been attributed to the increased risk of cancer and infectious diseases in individuals experiencing psychological stress.
Atopic dermatitis (AD) is characterized by elevated serum levels of allergen-specific IgE, cutaneous inflammation with infiltration of eosinophils, and enhanced expression of type 2 cytokines in inflamed tissues. When AD patients experience psychological stress, such as anxiety, their eosinophil counts in the peripheral blood increase, along with serum IgE titers and reduced TH1/TH2 ratios.
About the study
The current study investigates the molecular mechanisms